Hydroxycitric acid reconstructs damaged articular cartilages by modifying the metabolic cascade in chondrogenic cells

Osteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal stem cells (MSCs) provide a cell source for chondrogenic cells, we hypothesize that chemicals capable of enhancing the chondrogenic potential of MSCs w...

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Published inOsteoarthritis and cartilage open Vol. 7; no. 1; p. 100564
Main Authors Mizushina, Yoshiyuki, Sun, Liping, Nishio, Megumi, Nagata, Sanae, Kamakura, Takeshi, Fukuda, Masayuki, Tanaka, Kousuke, Toguchida, Junya, Jin, Yonghui
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.03.2025
Elsevier
Subjects
ATP citrate lyase
Chondrogenesis
Hydroxycitric acid
Mitochondria
ORIGINAL PAPER
Osteoarthritis
β-catenin
ATP citrate lyase
DM-α-KG
OXPHOS
FCCP
WB
TMRE
FGF2
ActA
β-catenin
iPSCs
ACAN
LC-MS/MS
Mitochondria
OA
CPII
C2C
α-KG
FBS
Ac-CoA
Hydroxycitric acid
Chondrogenesis
RT-qPCR
Hyp
CP4H
PBS
2D-CI
TSA
BM-MSCs
HCA
IP
3D-CI
GAG
EDTA
ECAR
BMPs
ACLY
COL2A1
iMSCs
TGFβ
Osteoarthritis
HE
PN
dsDNA
OCR
Online AccessGet full text

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Abstract Osteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal stem cells (MSCs) provide a cell source for chondrogenic cells, we hypothesize that chemicals capable of enhancing the chondrogenic potential of MSCs with transforming growth factor-beta (TGFβ) in vitro may similarly promote chondrogenesis in articular cartilage in vivo. Chemical compounds that enhance the TGFβ signaling for chondrogenesis were investigated utilizing mesenchymal stem cells derived from human induced pluripotent stem cells. The mechanisms of action underlying the identified compound were explored in vitro, and its therapeutic effects were validated in vivo using a mouse model of exercise-induced osteoarthritis. Hydroxycitric acid (HCA) emerged as the lead compound. In vitro, HCA effectively enhanced chondrogenesis by inhibiting ATP citrate lyase, inducing citrate and alpha-ketoglutarate (α-KG), while reducing cytosolic acetyl coenzyme A (Ac-CoA). This induction of α-KG promoted collagen prolyl-4-hydroxylase activity, boosting hydroxyproline production and matrix formation. The reduction of Ac-CoA attenuated the inhibitory effect of β-catenin on mitochondrial activity by diminishing its acetylation. In vivo, orally administered HCA accumulated in joint tissues of mice and histological examination demonstrated newly synthesized cartilage tissues in damaged area. Analysis of joint tissue extracts revealed a downregulation of Ac-CoA and an upregulation of citrate and α-KG, accompanied by a systemic increase in an anabolic biomarker. HCA demonstrates promise as an osteoarthritis therapy by enhancing chondrogenic differentiation. Its ability to modulate crucial metabolic pathways and facilitate cartilage repair suggests potential for clinical translation, addressing a critical need in the treatment of osteoarthritis.
AbstractList Osteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal stem cells (MSCs) provide a cell source for chondrogenic cells, we hypothesize that chemicals capable of enhancing the chondrogenic potential of MSCs with transforming growth factor-beta (TGFβ) in vitro may similarly promote chondrogenesis in articular cartilage in vivo.ObjectiveOsteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal stem cells (MSCs) provide a cell source for chondrogenic cells, we hypothesize that chemicals capable of enhancing the chondrogenic potential of MSCs with transforming growth factor-beta (TGFβ) in vitro may similarly promote chondrogenesis in articular cartilage in vivo.Chemical compounds that enhance the TGFβ signaling for chondrogenesis were investigated utilizing mesenchymal stem cells derived from human induced pluripotent stem cells. The mechanisms of action underlying the identified compound were explored in vitro, and its therapeutic effects were validated in vivo using a mouse model of exercise-induced osteoarthritis.DesignChemical compounds that enhance the TGFβ signaling for chondrogenesis were investigated utilizing mesenchymal stem cells derived from human induced pluripotent stem cells. The mechanisms of action underlying the identified compound were explored in vitro, and its therapeutic effects were validated in vivo using a mouse model of exercise-induced osteoarthritis.Hydroxycitric acid (HCA) emerged as the lead compound. In vitro, HCA effectively enhanced chondrogenesis by inhibiting ATP citrate lyase, inducing citrate and alpha-ketoglutarate (α-KG), while reducing cytosolic acetyl coenzyme A (Ac-CoA). This induction of α-KG promoted collagen prolyl-4-hydroxylase activity, boosting hydroxyproline production and matrix formation. The reduction of Ac-CoA attenuated the inhibitory effect of β-catenin on mitochondrial activity by diminishing its acetylation. In vivo, orally administered HCA accumulated in joint tissues of mice and histological examination demonstrated newly synthesized cartilage tissues in damaged area. Analysis of joint tissue extracts revealed a downregulation of Ac-CoA and an upregulation of citrate and α-KG, accompanied by a systemic increase in an anabolic biomarker.ResultsHydroxycitric acid (HCA) emerged as the lead compound. In vitro, HCA effectively enhanced chondrogenesis by inhibiting ATP citrate lyase, inducing citrate and alpha-ketoglutarate (α-KG), while reducing cytosolic acetyl coenzyme A (Ac-CoA). This induction of α-KG promoted collagen prolyl-4-hydroxylase activity, boosting hydroxyproline production and matrix formation. The reduction of Ac-CoA attenuated the inhibitory effect of β-catenin on mitochondrial activity by diminishing its acetylation. In vivo, orally administered HCA accumulated in joint tissues of mice and histological examination demonstrated newly synthesized cartilage tissues in damaged area. Analysis of joint tissue extracts revealed a downregulation of Ac-CoA and an upregulation of citrate and α-KG, accompanied by a systemic increase in an anabolic biomarker.HCA demonstrates promise as an osteoarthritis therapy by enhancing chondrogenic differentiation. Its ability to modulate crucial metabolic pathways and facilitate cartilage repair suggests potential for clinical translation, addressing a critical need in the treatment of osteoarthritis.ConclusionsHCA demonstrates promise as an osteoarthritis therapy by enhancing chondrogenic differentiation. Its ability to modulate crucial metabolic pathways and facilitate cartilage repair suggests potential for clinical translation, addressing a critical need in the treatment of osteoarthritis.
Osteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal stem cells (MSCs) provide a cell source for chondrogenic cells, we hypothesize that chemicals capable of enhancing the chondrogenic potential of MSCs with transforming growth factor-beta (TGFβ) in vitro may similarly promote chondrogenesis in articular cartilage in vivo. Chemical compounds that enhance the TGFβ signaling for chondrogenesis were investigated utilizing mesenchymal stem cells derived from human induced pluripotent stem cells. The mechanisms of action underlying the identified compound were explored in vitro, and its therapeutic effects were validated in vivo using a mouse model of exercise-induced osteoarthritis. Hydroxycitric acid (HCA) emerged as the lead compound. In vitro, HCA effectively enhanced chondrogenesis by inhibiting ATP citrate lyase, inducing citrate and alpha-ketoglutarate (α-KG), while reducing cytosolic acetyl coenzyme A (Ac-CoA). This induction of α-KG promoted collagen prolyl-4-hydroxylase activity, boosting hydroxyproline production and matrix formation. The reduction of Ac-CoA attenuated the inhibitory effect of β-catenin on mitochondrial activity by diminishing its acetylation. In vivo, orally administered HCA accumulated in joint tissues of mice and histological examination demonstrated newly synthesized cartilage tissues in damaged area. Analysis of joint tissue extracts revealed a downregulation of Ac-CoA and an upregulation of citrate and α-KG, accompanied by a systemic increase in an anabolic biomarker. HCA demonstrates promise as an osteoarthritis therapy by enhancing chondrogenic differentiation. Its ability to modulate crucial metabolic pathways and facilitate cartilage repair suggests potential for clinical translation, addressing a critical need in the treatment of osteoarthritis.
Objective: Osteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal stem cells (MSCs) provide a cell source for chondrogenic cells, we hypothesize that chemicals capable of enhancing the chondrogenic potential of MSCs with transforming growth factor-beta (TGFβ) in vitro may similarly promote chondrogenesis in articular cartilage in vivo. Design: Chemical compounds that enhance the TGFβ signaling for chondrogenesis were investigated utilizing mesenchymal stem cells derived from human induced pluripotent stem cells. The mechanisms of action underlying the identified compound were explored in vitro, and its therapeutic effects were validated in vivo using a mouse model of exercise-induced osteoarthritis. Results: Hydroxycitric acid (HCA) emerged as the lead compound. In vitro, HCA effectively enhanced chondrogenesis by inhibiting ATP citrate lyase, inducing citrate and alpha-ketoglutarate (α-KG), while reducing cytosolic acetyl coenzyme A (Ac-CoA). This induction of α-KG promoted collagen prolyl-4-hydroxylase activity, boosting hydroxyproline production and matrix formation. The reduction of Ac-CoA attenuated the inhibitory effect of β-catenin on mitochondrial activity by diminishing its acetylation. In vivo, orally administered HCA accumulated in joint tissues of mice and histological examination demonstrated newly synthesized cartilage tissues in damaged area. Analysis of joint tissue extracts revealed a downregulation of Ac-CoA and an upregulation of citrate and α-KG, accompanied by a systemic increase in an anabolic biomarker. Conclusions: HCA demonstrates promise as an osteoarthritis therapy by enhancing chondrogenic differentiation. Its ability to modulate crucial metabolic pathways and facilitate cartilage repair suggests potential for clinical translation, addressing a critical need in the treatment of osteoarthritis.
ArticleNumber 100564
Author Mizushina, Yoshiyuki
Nagata, Sanae
Toguchida, Junya
Sun, Liping
Kamakura, Takeshi
Fukuda, Masayuki
Jin, Yonghui
Nishio, Megumi
Tanaka, Kousuke
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  givenname: Liping
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  organization: Department of Regeneration Sciences and Engineering, Institute for Life and Medical Sciences, Kyoto University, 53 Shogoin-Kawahara-cho, Sakyo-Ku, Kyoto, 606-8507, Japan
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  givenname: Megumi
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  givenname: Sanae
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– sequence: 6
  givenname: Masayuki
  surname: Fukuda
  fullname: Fukuda, Masayuki
  organization: Department of Regeneration Sciences and Engineering, Institute for Life and Medical Sciences, Kyoto University, 53 Shogoin-Kawahara-cho, Sakyo-Ku, Kyoto, 606-8507, Japan
– sequence: 7
  givenname: Kousuke
  surname: Tanaka
  fullname: Tanaka, Kousuke
  organization: Central R & D Laboratory, Kobayashi Pharmaceutical Co., Ltd., 1-30-3 Toyokawa, Ibaraki, 567-0057, Japan
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  givenname: Junya
  surname: Toguchida
  fullname: Toguchida, Junya
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  givenname: Yonghui
  orcidid: 0000-0002-7095-8295
  surname: Jin
  fullname: Jin, Yonghui
  email: jinyh@cira.kyoto-u.ac.jp
  organization: Department of Regeneration Sciences and Engineering, Institute for Life and Medical Sciences, Kyoto University, 53 Shogoin-Kawahara-cho, Sakyo-Ku, Kyoto, 606-8507, Japan
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Issue 1
Keywords ATP citrate lyase
DM-α-KG
OXPHOS
FCCP
WB
TMRE
FGF2
ActA
β-catenin
iPSCs
ACAN
LC-MS/MS
Mitochondria
OA
CPII
C2C
α-KG
FBS
Ac-CoA
Hydroxycitric acid
Chondrogenesis
RT-qPCR
Hyp
CP4H
PBS
2D-CI
TSA
BM-MSCs
HCA
IP
3D-CI
GAG
EDTA
ECAR
BMPs
ACLY
COL2A1
iMSCs
TGFβ
Osteoarthritis
HE
PN
dsDNA
OCR
Language English
License This is an open access article under the CC BY license.
2024 The Author(s).
This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
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PublicationTitle Osteoarthritis and cartilage open
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Snippet Osteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal stem cells...
Objective: Osteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal...
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SubjectTerms ATP citrate lyase
Chondrogenesis
Hydroxycitric acid
Mitochondria
ORIGINAL PAPER
Osteoarthritis
β-catenin
Title Hydroxycitric acid reconstructs damaged articular cartilages by modifying the metabolic cascade in chondrogenic cells
URI https://dx.doi.org/10.1016/j.ocarto.2024.100564
https://www.ncbi.nlm.nih.gov/pubmed/39835169
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